A central role for S-nitrosothiols in plant disease resistance

A. Feechan, E. -J. Kwon, B. -Y. Yuri, Y. Wang, J. A. Pallas, G. J. Loake

Research output: Contribution to journalArticlepeer-review

Abstract

Animal 5-nitrosoglutathione reductase (GSNOR) governs the extent of cellular S-nitrosylation, a key redox-based posttranslational modification. Mutations in AtGSNOR1, an Arabidopsis thaliana GSNOR, modulate the extent of cellular S-nitrosothiol (SNO) formation in this model plant species. Loss of AtGSNOR1 function increased SNO levels, disabling plant defense responses conferred by distinct resistance (R) gene subclasses. Furthermore, in the absence of AtGSNOR1, both basal and nonhost disease resistance are also compromised. Conversely, increased AtGSNOR1 activity reduced SNO formation, enhancing protection against ordinarily virulent microbial pathogens. Here we demonstrate that AtGSNOR1 positively regulates the signaling network controlled by the plant immune system activator, salicylic acid. This contrasts with the function of this enzyme in mice during endotoxic shock, where GSNOR antagonizes inflammatory responses. Our data imply SNO formation and turnover regulate multiple modes of plant disease resistance.

Original languageEnglish
Pages (from-to)8054-8059
Number of pages6
JournalProceedings of the National Academy of Sciences
Volume102
Issue number22
DOIs
Publication statusPublished - 31 May 2005

Keywords

  • S-nitrosylation
  • salicylic acid
  • nitric oxide

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